Bottom Line:
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure.In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed.The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05).

ABSTRACTJia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent. In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed. CF proliferation was significantly increased in the Ang II‑treated group, compared with the control group (P<0.05). The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05). Following JSDS treatment, the increased levels of collagen and cell proliferation were inhibited, and the increased expression levels of p‑Smad2 and p‑Smad3 were also inhibited (P<0.05). These data suggested that JSDS may inhibit CF proliferation via attenuating the TGF‑β1/Smad signaling pathway.

Mentions:
Previous studies have shown that CFs may promote the development of fibrosis by producing fibrosis-associated factors, including collagen I and III (29–31). The enhancement of collagen I and III represent the predominant phenotype in cardiac fibrosis. Therefore, the present study examined whether JSDS suppressed collagen synthesis following Ang II stimulation. Compared with the control group, Ang II significantly increased the mRNA expression of collagen I. The mRNA expression of collagen I was downregulated following pre-treatment with JSDS (Fig. 4A). Immunofluorescence staining showed that JSDS inhibited the protein expression of collagen I in the CFs (Fig. 4B and C). Taken together, these findings indicated that the CFs treated with Ang II had enhanced secretory effects and that JSDS may prevent the increased protein expression of collagen I.

Mentions:
Previous studies have shown that CFs may promote the development of fibrosis by producing fibrosis-associated factors, including collagen I and III (29–31). The enhancement of collagen I and III represent the predominant phenotype in cardiac fibrosis. Therefore, the present study examined whether JSDS suppressed collagen synthesis following Ang II stimulation. Compared with the control group, Ang II significantly increased the mRNA expression of collagen I. The mRNA expression of collagen I was downregulated following pre-treatment with JSDS (Fig. 4A). Immunofluorescence staining showed that JSDS inhibited the protein expression of collagen I in the CFs (Fig. 4B and C). Taken together, these findings indicated that the CFs treated with Ang II had enhanced secretory effects and that JSDS may prevent the increased protein expression of collagen I.

Bottom Line:
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure.In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed.The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05).

ABSTRACTJia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent. In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed. CF proliferation was significantly increased in the Ang II‑treated group, compared with the control group (P<0.05). The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05). Following JSDS treatment, the increased levels of collagen and cell proliferation were inhibited, and the increased expression levels of p‑Smad2 and p‑Smad3 were also inhibited (P<0.05). These data suggested that JSDS may inhibit CF proliferation via attenuating the TGF‑β1/Smad signaling pathway.